Estrogen, the load-bearing one

Estrogen tells the bone-resorbing cells (osteoclasts) to slow down. When estradiol drops at menopause, osteoclasts speed up and start removing bone faster than the bone-building cells (osteoblasts) can replace it. The first 5 years post-menopause is where most women lose the most bone density they will ever lose — typically 1 to 2 per cent per year of trabecular bone, more if periods stopped before 45.

This is why MHT started within 10 years of the final period reliably preserves bone density and reduces hip and vertebral fractures. It is also why a baseline DEXA scan is reasonable for any woman with early menopause, low body weight, eating disorder history, long steroid use, or a family history of hip fracture.

Estrogen receptors are dense in the hippocampus, prefrontal cortex, and amygdala — the regions that handle verbal memory, executive function and emotional regulation. As estradiol falls, glucose uptake in some of these regions measurably drops on PET imaging. That is the biological basis for the word-finding pauses, the lost-thread feeling, the slower processing in meetings.

For most women, the cognitive changes ease 1 to 2 years after the final period as the brain re-equilibrates. For a smaller group they don't, and for women with strong family histories of dementia the long-game question of MHT and brain health is genuinely unsettled — there is signal that early-window MHT may be neutral-to-protective for Alzheimer's risk, and signal that late-start MHT may be the opposite. Worth a frank conversation with a menopause-trained doctor, not a forum.

Genitourinary syndrome of menopause (GSM) is the umbrella term for vaginal dryness, painful sex, urinary urgency, post-coital UTIs, and the thinning of vulvar skin. Up to 80 per cent of postmenopausal women develop it, and unlike hot flashes it does not pass with time — it gets steadily worse without treatment.

Topical (vaginal) estrogen — cream, ring, or pessary — is the standard of care, with very low systemic absorption and a reassuring safety profile even in many women who can't take systemic MHT. It is consistently rated one of the highest-impact, lowest-risk treatments in menopause care and is consistently under-prescribed.

The 2002 Women's Health Initiative headline — 'a 26 per cent increase in breast cancer risk on combined HRT' — was a relative risk on conjugated equine estrogen plus medroxyprogesterone acetate (MPA), in women with an average age of 63. The absolute number was about 8 extra cases per 10 000 women per year — smaller than the risk attributed to drinking two glasses of wine a night or being five units of BMI heavier.

Estrogen-only MHT (for women without a uterus) did not increase breast cancer risk in WHI and may have lowered it slightly. More recent observational data suggest that body-identical micronised progesterone carries a smaller breast signal than older synthetic progestins, particularly in the first 5 years of use. The honest sentence is 'small absolute increase, mostly tied to specific synthetic progestins, mostly after several years of use', not 'HRT causes breast cancer'.